Neuroscience letters
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Neuroscience letters · Jan 1998
Pre-emptive intrathecal Mk-801, a non-competitive N-methyl-D-aspartate receptor antagonist, inhibits the up-regulation of spinal dynorphin mRNA and hyperalgesia in a rat model of chronic inflammation.
The effects of N-methyl-D-aspartate(NMDA) receptor antagonist, Mk-801, on the expression of spinal dynorphin (DYN) mRNA and the hyperalgesia induced by peripheral inflammation were studied by Northern analysis and behavioral test. Following an unilateral injection of complete Freund's adjuvant (CFA) into the rat hindpaw, there appeared a significant hyperalgesia of inflamed hindpaw and up-regulation of ipsilateral spinal DYN mRNA; while the pre-emptive and continuous intrathecal administration of Mk-801 (10 microg/microl per h) could significantly suppress both the hyperalgesia and the up-regulation of spinal DYN mRNA induced by peripheral inflammation. The results suggest that NMDA receptor activation may contribute to the development and maintenance of the thermal hyperalgesia that is associated with the up-regulation of DYN expression in spinal dorsal horn.
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Neuroscience letters · Nov 1997
Formalin injection in the tail facilitates hindpaw withdrawal reflexes induced by thermal stimulation in the rat: effect of paracetamol.
With the aim to develop a simple behavioural method for the study of hyperalgesic processes and for the evaluation of anti-hyperalgesic properties of analgesic drugs, the effect of the tail injection of formalin (10% formaldehyde intradermally) on hindpaw nociceptive thresholds to thermal stimulation was evaluated in the rat. The formalin injection in the tail induced a significant reduction of plantar test latencies. ⋯ However, this drug was unable to block hyperalgesia when already established. Our results suggest that this method could be used for the evaluation of analgesic drugs in an experimental setting representative of clinical pain.
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Neuroscience letters · Oct 1997
Generalised seizure-induced changes in rat hippocampal glutamate but not GABA release are potentiated by repeated seizures.
The effects of repeated or a single generalised seizure on extracellular glutamate and gamma-aminobutyric acid (GABA) levels in the ventral hippocampus of the freely-moving rat were studied using maximal electroshock-induced seizures in conjunction with in vivo microdialysis. A single seizure resulted in three phases of post-ictal changes in glutamate and GABA levels: during phase I, there were transient increases in both glutamate and GABA whilst in phase II, levels of both amino acids were reduced. ⋯ Following repeated seizures, the phase I rise in glutamate was increased 3-fold and the phase III rise was significantly potentiated, compared with the changes produced by a single seizure. No differences were observed in the post-ictal changes in GABA levels between a single or repeated seizures.
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Neuroscience letters · Jul 1997
The decreased susceptibility to the development of in vitro kindling-like state in hippocampal CA1 slices of rats sensitive to audiogenic seizures.
The field excitatory postsynaptic potential (fEPSP) with the presynaptic fiber volley (PrV) and the population spike (PS) were recorded with two glass microelectrodes in stratum radiatum and stratum pyramidale of rat hippocampal CA1 slices, respectively, in response to electric stimulation of Schaffer collaterals/commissural fibers (SC/CF) containing glutamate as a neurotransmitter. Three components of the overall input-output function were taken: (1) PrV amplitude vs. intensity of stimulating current, (2) dendritic layer fEPSP slope vs. PrV amplitude and (3) PS amplitude vs. fEPSP slope. ⋯ Such short-term [K+]o increases also did not induce the EPSP-spike transfer potentiation (E-S potentiation) in CA1 pyramidal neurons of audiogenic rats either. Furthermore, the presynaptic glutamatergic fibers of GPAS rats are less excitable to stimulating currents then that of normal Wistar rats. It is suggested that the resistance of audiogenic rat hippocampal CAI slices to the development of long lasting epileptiform activity is a protective adaptive mechanism preventing the propagation of seizure activity into limbic structures.
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Neuroscience letters · Jul 1997
Destruction of neurokinin-1 receptor expressing cells in vitro and in vivo using substance P-saporin in rats.
Substance P (SP) acts on neurons through the neurokinin-1 (NK-1) receptor. Conjugation of SP to the ribosome inactivating protein, saporin (SAP), produces a cytotoxin selective for cells that express the NK-1 receptor. ⋯ Injection of SP-SAP into the striatum selectively destroyed NK-1 receptor expressing interneurons. These results show that SP-SAP will be useful for studying the function of NK-1 receptor expressing neurons.